Arthritis mutilans is a rare, severe form of inflammatory arthritis characterized by aggressive bone and joint destruction, most often affecting the hands and feet. In this condition, chronic inflammation leads to osteolysis (bone resorption) of the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints, causing digital shortening and deformities known as “opera-glass” or “telescoping” hands and feet WikipediaWikipedia. First described by Marie and Léri in 1913, it may also involve the spine, resulting in profound loss of joint architecture and function Wikipedia.
Arthritis mutilans is a rare, severe form of inflammatory arthritis most often seen in advanced psoriatic arthritis. In this condition, the immune system attacks the small joints—especially in the fingers and toes—causing extreme bone loss, joint destruction, and “pencil-in-cup” deformities on X-ray. Over time, this leads to shortening of the digits, marked functional impairment, and intense pain. Simple English: arthritis mutilans eats away the bone and cartilage so badly that fingers or toes can collapse and look shortened or deformed.
Pathophysiology involves chronic inflammation driven by cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-17 (IL-17), and IL-23. These molecules stimulate osteoclasts (bone-eating cells) and inhibit osteoblasts (bone-building cells), tipping the balance toward bone loss. Synovial tissue becomes hypertrophied (pannus formation), eroding cartilage and bone. Without prompt control of inflammation, joint spaces widen from bone resorption and collapse under mechanical stress.
Pathophysiologically, arthritis mutilans arises from unregulated activation of osteoclasts driven by proinflammatory cytokines (notably TNF-α, IL-17, and IL-23) in genetically susceptible individuals. This cytokine milieu promotes bone erosion and joint collapse, while attempts at new bone formation lead to ankylosis in later stages. Although the immunopathogenesis remains incompletely understood, genetic associations with HLA-B27 and IL-23 receptor variants have been demonstrated in psoriatic arthritis–associated cases Wikipedia.
Epidemiologically, arthritis mutilans occurs in approximately 5–16% of patients with psoriatic arthritis (PsA) and in fewer than 5% of all PsA cases; it is less common in rheumatoid arthritis (RA) but can arise in advanced, untreated disease MedlinePlusMedlinePlus. The condition typically presents in adults aged 30–50 but can occasionally occur in pediatric populations with juvenile idiopathic arthritis (JIA) PubMed. Early recognition and aggressive management are critical to prevent irreversible deformity and functional loss.
Types of Arthritis Mutilans
Arthritis mutilans is best classified by its underlying disease context or etiology. The major types include:
Psoriatic Arthritis Mutilans
This is the most common form, arising as the most severe subtype of PsA. It leads to rapid osteolysis of the DIP and PIP joints, producing “opera-glass” hands with skin creases folding over shortened phalanges. Bone marrow edema visible on MRI correlates with areas of active inflammation and bone erosion. Psoriatic pathology also often features nail pitting and dactylitis HealthlinePMC.Rheumatoid Arthritis Mutilans
Although rare, advanced RA can progress to an arthritis mutilans phenotype if uncontrolled. Chronic pannus formation erodes cartilage and bone, resulting in digital collapse and joint subluxation. Unlike PsA, RA-associated mutilans is commonly seropositive for rheumatoid factor (RF) and anti-CCP antibodies Wikipedia.Juvenile Idiopathic Arthritis Mutilans
In very rare cases, children with systemic or polyarticular JIA develop severe joint destruction akin to arthritis mutilans. Radiographs demonstrate carpal bone loss and ankylosis; early-onset PsA or RF-positive polyarticular JIA are risk factors. Case reports highlight the need for vigilant monitoring in pediatric rheumatology PubMedPubMed.Gouty Arthritis Mutilans
Chronic tophaceous gout can exceptionally present as arthritis mutilans. Monosodium urate crystal deposition provokes inflammation that, over years of poorly controlled hyperuricemia, leads to osteolysis and deformity. Recent case series document gouty mutilans in elderly patients with neglected tophaceous deposits PubMedPubMed.Other Inflammatory Arthropathies
Rarely, arthritis mutilans occurs in multicentric reticulohistiocytosis, systemic lupus erythematosus, systemic sclerosis, and infectious arthritis. In these contexts, severe soft-tissue proliferation or erosive changes mimic the classic deformities of PsA and RA mutilans Radiopaedia.
Causes of Arthritis Mutilans
Each of the following factors contributes to the development or progression of arthritis mutilans. Though the precise interplay varies by subtype, they represent key pathogenetic and risk factors:
Chronic Uncontrolled Inflammation
Persistent synovitis drives osteoclast activation, leading to bone resorption in affected joints Wikipedia.Genetic Susceptibility (HLA-B27, IL-23R)
Certain HLA alleles and cytokine receptor variants increase risk, particularly in psoriatic forms Wikipedia.High Proinflammatory Cytokine Levels
Elevated TNF-α, IL-17, and IL-23 correlate with more aggressive joint destruction PMC.Late Diagnosis or Delayed Treatment
Failure to initiate DMARDs or biologics early allows unchecked erosion over months to years Verywell Health.Smoking
Tobacco use augments systemic inflammation and may exacerbate joint damage Healthline.Obesity
Adipose-derived cytokines contribute to systemic inflammatory burden, worsening arthritic damage Healthline.Autoantibody Positivity (RF, Anti-CCP)
In RA-related cases, seropositive patients exhibit more erosive disease courses Wikipedia.High Acute-Phase Reactants (ESR, CRP)
Elevated markers at baseline predict radiographic progression PMC.Frequent Joint Trauma
Repeated microtrauma may lower the threshold for erosive damage Radiopaedia.Infectious Triggers
Bacterial arthritis (e.g., staphylococcal) can precipitate secondary mutilans changes in rare cases Radiopaedia.Metabolic Syndrome
Insulin resistance and dyslipidemia heighten inflammatory milieu Healthline.Psoriasis Severity
Extensive skin involvement correlates with higher risk of severe joint disease in PsA Healthline.Delayed Biologic Therapy
Hesitation to escalate to TNF inhibitors or IL-17 blockers allows further bone loss Wikipedia.Comorbid Autoimmune Disease
Coexistence of other autoimmune conditions (e.g., Sjögren’s) may amplify joint damage Radiopaedia.Advanced Age at Onset
Older age may portend more rapid progression due to diminished repair mechanisms Verywell Health.
Symptoms of Arthritis Mutilans
Patients with arthritis mutilans experience both local and systemic manifestations:
Severe Joint Pain
Persistent, deep aching pain in the hands or feet reflects active bone erosion Wikipedia.Swelling and Warmth
Inflamed synovium produces joint effusions and warmth on palpation Wikipedia.Digital Shortening
Osteolysis of phalanges leads to visibly shortened fingers or toes (“telescoping”) Wikipedia.Joint Deformity
Luxation, ankylosis, and bone collapse result in paw-like or opera-glass appearance Wikipedia.Limited Range of Motion
Structural loss and ankylosis severely restrict flexion and extension Wikipedia.Dactylitis (“Sausage Digit”)
Diffuse swelling of an entire finger or toe is common in psoriatic cases PMC.Nail Changes
Pitting, onycholysis, and ridging occur in PsA-associated mutilans Healthline.Functional Impairment
Patients struggle with grasping objects, walking, and fine motor tasks Verywell Health.Muscle Weakness
Disuse and pain lead to atrophy of intrinsic hand and foot muscles Verywell Health.Systemic Symptoms
Fatigue, low-grade fever, and malaise reflect chronic inflammatory state Verywell Health.
Diagnostic Tests for Arthritis Mutilans
Physical Exam
General Inspection
Observing hand and foot posture, skin folds, and deformities helps identify digital shortening and opera-glass appearance Wikipedia.Palpation for Tenderness & Warmth
Gently pressing joints reveals points of active inflammation and effusion Wikipedia.Range of Motion Assessment
Measuring flexion/extension loss quantifies functional impairment Wikipedia.Gait Analysis
Evaluating walking pattern detects forefoot mutilans effects on ambulation Verywell Health.Skin and Nail Examination
Checking for psoriatic plaques and nail pitting supports PsA-related diagnosis Healthline.
Manual Tests
Joint Squeeze Test
Compressing adjacent metacarpals elicits pain in inflamed joints Wikipedia.Telescoping Digit Test
Gently pulling on a finger demonstrates “sliding” phalanges characteristic of opera-glass hand Wikipedia.Stress Test for Joint Stability
Applying varus/valgus stress assesses collateral ligament integrity in PIP joints Verywell Health.
Lab & Pathological Tests
Erythrocyte Sedimentation Rate (ESR)
An elevated ESR indicates active systemic inflammation PMC.C-Reactive Protein (CRP)
High CRP correlates with radiographic progression in PsA mutilans PMC.Rheumatoid Factor (RF)
RF positivity supports RA-associated mutilans cases Wikipedia.Anti-CCP Antibodies
Highly specific for erosive RA forms, aiding differential diagnosis Wikipedia.HLA-B27 Typing
Identifies spondyloarthropathy-linked genetic risk in PsA mutilans Wikipedia.Synovial Fluid Analysis
Excludes infection and crystal arthropathy; shows inflammatory profile in mutilans Verywell Health.
Electrodiagnostic Tests
Nerve Conduction Studies
Detects peripheral neuropathy from entrapment in deformed digits Verywell Health.Electromyography (EMG)
Assesses muscle denervation secondary to joint deformities Verywell Health.
Imaging Tests
Plain Radiography (X-ray)
Reveals joint space loss, bone erosions, pencil-in-cup deformities, and telescoping digits PMC.Magnetic Resonance Imaging (MRI)
Detects bone marrow edema, synovitis, and early erosive changes not visible on X-ray Wikipedia.Computed Tomography (CT) Scan
Offers high-resolution images of bony architecture for pre-surgical planning PMC.Ultrasonography
Demonstrates synovial hypertrophy, power Doppler signals of active inflammation, and erosions in real time Wikipedia.
Non-Pharmacological Treatments
Physiotherapy and Electrotherapy Therapies
1. Therapeutic Ultrasound
Description: High-frequency sound waves applied via a gel-coated probe.
Purpose: To reduce deep inflammation and improve tissue healing.
Mechanism: Sound waves cause micro-vibrations in tissues, boosting blood flow and promoting anti-inflammatory effects through mild thermal heating.
2. Transcutaneous Electrical Nerve Stimulation (TENS)
Description: Gentle electrical currents delivered through skin electrodes.
Purpose: To block pain signals en route to the brain and stimulate endorphin release.
Mechanism: Activates large-fiber nerves that “close the gate” on pain transmission and trigger natural pain-relieving chemicals.
3. Shortwave Diathermy
Description: Deep-heating electromagnetic therapy.
Purpose: To ease pain and stiff joints by raising tissue temperature.
Mechanism: Electromagnetic waves heat tissues internally, relaxing muscles, improving blood flow, and reducing viscous synovial fluid.
4. Laser Therapy (Low-Level Laser Therapy)
Description: Non-thermal laser light applied to joints.
Purpose: To accelerate tissue repair and decrease inflammation.
Mechanism: Photons stimulate cellular mitochondria, boosting ATP production and triggering anti-inflammatory signaling.
5. Cryotherapy (Cold Packs)
Description: Application of cold to affected joints.
Purpose: To numb pain, reduce swelling, and slow nerve conduction.
Mechanism: Vasoconstriction limits inflammatory mediator release and decreases metabolic demand in tissues.
6. Heat Therapy (Hot Packs or Paraffin Wax)
Description: Superficial heat applied to skin.
Purpose: To relax stiff muscles and improve joint range of motion.
Mechanism: Increases local blood flow, decreases joint fluid viscosity, and soothes nerve endings.
7. Hydrotherapy (Aquatic Therapy)
Description: Exercise in warm water pools.
Purpose: To exercise joints with minimal weight and stress.
Mechanism: Buoyancy supports body weight, water resistance builds muscle gently, and warmth relaxes tissues.
8. Pulsed Electromagnetic Field Therapy (PEMF)
Description: Pulsed magnetic fields applied over joints.
Purpose: To promote cartilage repair and reduce inflammation.
Mechanism: Magnetic pulses influence ion exchange in cells, enhancing growth factor expression and reducing pro-inflammatory cytokines.
9. Shockwave Therapy
Description: Focused sound waves delivered to joint surfaces.
Purpose: To break down calcifications and stimulate healing.
Mechanism: Acoustic pulses induce microtrauma, triggering a healing response with new blood vessel growth and tissue remodeling.
10. Neuromuscular Electrical Stimulation (NMES)
Description: Electrical currents to elicit muscle contractions.
Purpose: To strengthen muscles around weakened joints.
Mechanism: Directly activates motor nerves, encouraging muscle hypertrophy and improved joint support.
Exercise Therapies
11. Range-of-Motion (ROM) Exercises
Description: Gentle joint movements taken through full motion.
Purpose: To maintain flexibility and prevent contractures.
Mechanism: Stretching synovial capsule and periarticular structures to preserve mobility.
12. Strengthening Exercises
Description: Resistance training with bands or light weights.
Purpose: To build muscle support around eroded joints.
Mechanism: Muscle fibers adapt to load by hypertrophying, increasing joint stability.
13. Aerobic Exercise
Description: Low-impact activities like cycling or walking.
Purpose: To improve cardiovascular health and reduce systemic inflammation.
Mechanism: Increases anti-inflammatory cytokines (e.g., IL-10) and decreases TNF-α levels.
14. Balance and Proprioception Training
Description: Exercises on wobble boards or single-leg stands.
Purpose: To reduce fall risk and improve joint coordination.
Mechanism: Enhances sensory feedback and neuromuscular control around damaged joints.
15. Aquatic Resistance Exercises
Description: Water-based strengthening against resistance currents.
Purpose: To strengthen muscles safely with minimal joint stress.
Mechanism: Water viscosity provides uniform multidirectional resistance, stimulating muscle growth.
Mind-Body Therapies
16. Mindfulness Meditation
Description: Focused breathing and awareness practice.
Purpose: To reduce pain perception and stress.
Mechanism: Lowers activity in brain pain centers and stress pathways (HPA axis), decreasing cortisol and inflammatory markers.
17. Yoga
Description: Gentle postures, breathing, and relaxation.
Purpose: To improve flexibility, balance, and mental well-being.
Mechanism: Combines stretching with parasympathetic activation, reducing muscle tension and systemic inflammation.
18. Biofeedback
Description: Real-time monitoring of physiological signals (e.g., muscle tension).
Purpose: To teach relaxation techniques and muscle control.
Mechanism: Visual or auditory feedback helps patients consciously reduce muscle tension and pain.
Educational Self-Management
19. Disease Education Workshops
Description: Structured group sessions on arthritis mutilans.
Purpose: To empower patients with knowledge for better self-care.
Mechanism: Understanding disease process and treatment options improves adherence and health outcomes.
20. Self-Monitoring and Goal-Setting
Description: Keeping a daily diary of symptoms, activity, and medication.
Purpose: To track triggers, progress, and treatment effectiveness.
Mechanism: Regular feedback helps adjust behaviors and share accurate data with clinicians.
Key Drugs for Arthritis Mutilans
1. Methotrexate
Class & Timing: Synthetic DMARD, 7.5–25 mg once weekly, orally or subcutaneously.
Dosage & Side Effects: Start at 7.5 mg/wk, increase gradually; monitor for liver toxicity, mouth sores, nausea, and bone marrow suppression.
2. Sulfasalazine
Class & Timing: Synthetic DMARD, 500 mg twice daily, orally.
Dosage & Side Effects: Titrate to 2 g/day; can cause gastrointestinal upset, rash, and reversible oligospermia.
3. Leflunomide
Class & Timing: Synthetic DMARD, 20 mg once daily, orally.
Dosage & Side Effects: Loading dose optional; monitor for hepatotoxicity, hypertension, and hair thinning.
4. Hydroxychloroquine
Class & Timing: Synthetic DMARD, 200–400 mg once daily, orally.
Dosage & Side Effects: Retinal toxicity risk—annual eye exams required; gastrointestinal upset and headache possible.
5. Etanercept
Class & Timing: TNF inhibitor biologic, 50 mg once weekly, subcutaneously.
Dosage & Side Effects: Risk of infection, injection-site reactions, and rare demyelinating disease.
6. Infliximab
Class & Timing: TNF inhibitor biologic, 5 mg/kg at weeks 0, 2, 6, then every 8 weeks, IV infusion.
Dosage & Side Effects: Infusion reactions, infection risk, and possible heart failure exacerbation.
7. Adalimumab
Class & Timing: TNF inhibitor biologic, 40 mg every other week, subcutaneously.
Dosage & Side Effects: Similar to etanercept—monitor for infections and lupus-like syndrome.
8. Secukinumab
Class & Timing: IL-17A inhibitor, 150–300 mg at weeks 0, 1, 2, 3, 4, then monthly, subcutaneously.
Dosage & Side Effects: Risk of candida infections, nasopharyngitis, and inflammatory bowel disease flare.
9. Apremilast
Class & Timing: PDE4 inhibitor, 30 mg twice daily, orally.
Dosage & Side Effects: Diarrhea, headache, weight loss; fewer infection risks than biologics.
10. Tofacitinib
Class & Timing: JAK inhibitor, 5 mg twice daily, orally.
Dosage & Side Effects: Monitor for infections, lipid changes, and rare blood clots.
Dietary Molecular Supplements
1. Glucosamine Sulfate (1500 mg/day)
Supports cartilage structure by providing building blocks. Inhibits enzymes that break down cartilage.
2. Chondroitin Sulfate (1200 mg/day)
Attracts water into cartilage, improving shock absorption. Blocks destructive enzymes and reduces inflammation.
3. Omega-3 Fatty Acids (2–3 g EPA/DHA daily)
Anti-inflammatory by competing with arachidonic acid for enzyme binding, decreasing pro-inflammatory prostaglandins.
4. Vitamin D₃ (1000–2000 IU/day)
Modulates immune response, reduces pro-inflammatory cytokines, and supports bone health.
5. Curcumin (500–2000 mg/day)
Blocks NF-κB pathway, reducing production of TNF-α and IL-1β.
6. Methylsulfonylmethane (MSM) (1.5–3 g/day)
Provides sulfur for collagen synthesis and reduces oxidative stress in joints.
7. Boswellia Serrata Extract (300–600 mg frankincense-resin daily)
Inhibits 5-lipoxygenase enzyme, cutting down leukotriene-mediated inflammation.
8. Ginger Extract (500–1000 mg/day)
Blocks COX and LOX pathways, reducing production of pro-inflammatory mediators.
9. Collagen Peptides (10 g/day)
Supplies amino acids for cartilage repair and stimulates chondrocyte activity.
10. Vitamin C (500–1000 mg/day)
Essential cofactor in collagen synthesis and antioxidant, protecting joint tissues from free radicals.
Advanced or Regenerative Agents
1. Alendronate (70 mg once weekly)
Bisphosphonate that binds bone mineral, inhibiting osteoclast-mediated bone resorption to preserve joint bone stock.
2. Risedronate (35 mg once weekly)
Similar to alendronate; reduces bone turnover and erosion progression.
3. Platelet-Rich Plasma (PRP) Injections
3–5 mL per joint, repeated monthly; concentrates growth factors that stimulate cartilage repair and reduce inflammation.
4. Autologous Conditioned Serum (ACS)
2 mL intra-articular; enriched in IL-1 receptor antagonist to counteract IL-1β–driven cartilage breakdown.
5. Hyaluronic Acid (Viscosupplementation, 20 mg weekly × 3–5 weeks)
Restores synovial fluid viscosity, lubricating the joint and reducing pain.
6. Mesenchymal Stem Cell Therapy
~10–20 million cells via intra-articular injection; promotes regeneration by differentiating into cartilage cells and secreting anti-inflammatory factors.
5 Surgical Options
Synovectomy
Removal of inflamed synovium through open or arthroscopic surgery. Benefits: reduces pain, slows joint damage, and may delay more extensive surgery.
2. Arthrodesis (Joint Fusion)
Fuses the destroyed joint surfaces, typically in toes or fingers, using plates or screws. Benefits: eliminates painful movement and stabilizes deformity.
3. Joint Replacement Arthroplasty
Replacing severely damaged joints (e.g., MCP joint) with prosthetic implants. Benefits: restores function, relieves pain, and corrects deformity.
4. Corrective Osteotomy
Bone cutting to realign severely deformed digits. Benefits: improves joint alignment, function, and hand posture.
5. Tendon Transfer
Repositions tendons to compensate for lost joint function. Benefits: enhances grip strength and fine motor control.
Prevention Strategies
Early Diagnosis and Treatment: Start DMARDs at first sign of severe psoriatic arthritis to prevent mutilans.
Smoking Cessation: Smoking increases inflammation and disease progression; quitting slows joint damage.
Weight Management: Reduces mechanical stress on joints and lowers systemic inflammation.
Regular Low-Impact Exercise: Keeps joints flexible without overloading damaged areas.
Balanced Anti-Inflammatory Diet: Rich in omega-3s, antioxidants, and fiber to curb chronic inflammation.
Joint Protection Techniques: Use adaptive aids (e.g., jar openers) to avoid excessive joint strain.
Periodic Imaging and Lab Monitoring: X-rays, MRI, CRP/ESR checks to catch progression early.
Stress Management: High stress can trigger flares; use relaxation techniques.
Adequate Sleep: Restorative sleep supports immune regulation and tissue repair.
Limit Alcohol Intake: Excessive alcohol can worsen inflammation and interfere with medications.
When to See a Doctor
Seek medical attention promptly if you experience rapidly worsening joint pain, new deformities, inability to grip or walk, signs of systemic illness (fever, weight loss), or if you notice red, swollen joints lasting more than a week despite home care. Early referral to a rheumatologist is crucial—delaying can lead to irreversible bone loss and disability.
Self-Care: Things to Do and 10 Things to Avoid
What to Do
Apply heat or cold packs to soothe painful joints daily.
Follow your prescribed exercise program for strength and flexibility.
Keep a symptom diary and share it with your doctor.
Take medications exactly as directed; never skip a dose.
Use ergonomic tools (e.g., jar openers, padded grips) to protect joints.
Practice stress-reducing activities like meditation or gentle yoga.
Maintain a healthy weight through diet and activity.
Attend regular check-ups for labs and imaging.
Sleep on a supportive mattress and pillow.
Stay hydrated to support joint lubrication.
What to Avoid
High-impact sports (e.g., running, jumping) that overload joints.
Repetitive hand or foot motions without breaks.
Smoking or exposure to secondhand smoke.
Excessive alcohol, which can worsen inflammation.
Skipping medications when you feel better.
Ignoring new or worsening pain.
Crash diets that lack nutrients for joint health.
Carrying heavy loads without proper support.
Inactive lifestyle—avoid long periods of immobility.
Self-medicating with unproven supplements.
Frequently Asked Questions
1. What is arthritis mutilans?
Arthritis mutilans is the most destructive form of psoriatic arthritis, leading to severe bone loss and joint collapse, especially in the fingers and toes.
2. What causes arthritis mutilans?
It arises when chronic immune-driven inflammation (via TNF-α, IL-17, IL-23) overactivates osteoclasts, eroding bone and cartilage faster than it can be repaired.
3. How is it diagnosed?
Diagnosis is based on clinical signs (deforming joints, severe pain), blood tests (CRP, ESR), and characteristic X-ray findings like “pencil-in-cup” deformities.
4. Can arthritis mutilans be cured?
There’s no cure, but early and aggressive treatment with DMARDs and biologics can halt progression and preserve joint function.
5. How effective are non-drug therapies?
Physiotherapy, exercise, and mind-body approaches can significantly reduce pain, improve mobility, and enhance quality of life when used alongside medications.
6. Are supplements helpful?
Supplements like glucosamine, omega-3s, and curcumin may provide modest anti-inflammatory benefits, but they should complement—not replace—medical treatments.
7. When is surgery needed?
Surgery is reserved for joints with irreversible damage causing pain or severe deformity unresponsive to conservative care.
8. Is arthritis mutilans hereditary?
A genetic predisposition exists, especially with psoriasis, but environmental factors like smoking also play a major role.
9. Can exercise worsen my joints?
High-impact exercises can harm damaged joints. Low-impact, guided exercises are safe and recommended to maintain function.
10. What lifestyle changes help?
Quitting smoking, maintaining healthy weight, balanced diet rich in anti-inflammatory nutrients, and good sleep hygiene all support joint health.
11. How often should I see my rheumatologist?
Every 3–6 months if stable, or more frequently during flares or medication changes.
12. Are biologic drugs safe long-term?
Generally yes, but regular monitoring for infections, blood counts, and rare adverse effects is essential.
13. Can children get arthritis mutilans?
Juvenile psoriatic arthritis can rarely progress to mutilans; early pediatric rheumatology care is vital.
14. How do I manage daily activities?
Use assistive devices, pace tasks, take frequent breaks, and apply protective splints as needed.
15. What research is underway?
New biologics targeting IL-17, IL-23, and JAK pathways, plus regenerative therapies like stem cells and PRP, show promise for future treatment.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: July 11, 2025.
